5Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Applicant’s arguments and amendments filed on 3/2/2026 have been entered.
Claims 37 and 38 have been amended.
The objection to claims 37 and 38 are withdrawn in view of Applicants’ amendments.
The rejection of claim 39 under 112b is withdrawn in view of Applicant’s amendments
Claims 37-41 are examined in the instant application.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claim(s) 37-39 remain rejected under 35 U.S.C. 103 as being unpatentable over Rosa et al. (December 2018, Science Immunology, Vol. 3, pgs. 1-15, cited on IDS 8/24/2022) in view of Zeng et al. (2015, Mucosal Immunology, Vol. 9(1), pgs. 183-193, cited on IDS 8/24/2022) and evidenced by Deneault et al. (US 20090215875 A1), Chicz et al. (WO 2002/078524 A1) and Jain et al. (WO2013/070563 A1) for reasons of record in the Non-Final Office Action mailed on 12/1/2025 (and repeated below as amended).
Regarding claim 37, Rosa et al. teach a method of reprogramming human and mouse fibroblasts to conventional type 2 dendritic cells (cDC2) via transduction with a vector expressing a combination of transcription factors comprising PU.1 IRF4 and IRF8; and
culturing the transduced fibroblasts in a cell media, for at least two days, that supports the growth of dendritic cells (see Abstract, pg. 1 col. 2, Fig. 3G and pg. 12 col. 1 parag. 1).
While the majority of dendritic cells produced by Rosa were type 1 (cDC1-Fig. 3G), to generate cDC2 cells in the method of Rosa, it would be obvious to use a transcription factor such as PRDM1.
Rosa does not teach:
using a third transcription factor such as PRDM1.
Regarding using PRDM1 to reprogram cells to cDC2’s, Zeng et al. teach a
comparison of transcription factors that specify a cDC1 vs cDC2 phenotype and discovered that PRDM1 is upregulated in cDC2 cells and downregulated in cDC1 cells (pg. 190 col. 1 parag. 2 and pg. 191 col. 2 parag. 2 lines 8-11).
Importantly. Zeng teaches that the transcription factor IRF8 fates a dendritic cell towards type 1 and Blimp-1 (aka PRDM1) fates a cell towards type 2 (pg. 191 col. 2 parag. 2 lines 1-4).
As set forth below the sequences for the transcription factors used by Rosa and Zeng, PU.1, IRF4 and PRDM1, were all known at the time of filing.
Regarding SEQ ID NO: 3 (PU.1), Denault et al. teach a sequence 100% identical to instant SEQ ID NO: 3.
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Regarding SEQ ID NO: 9 (IRF4), Chicz et al. teach a sequence 100% identical to instant SEQ ID NO: 9.
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Regarding SEQ ID NO: 15 (PRDM1), Jain et al. teach a sequence 100% identical to instant SEQ ID NO: 15.
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Thus, at the time of filing the ordinary artisan would have found it prima facie obvious to modify the teachings of Rosa regarding using the transcription factors PU.1, IRF4 and IRF8 to obtain cDC1 and cDC2 cells with the teachings of Zeng regarding the transcription factor PRDM1 and its role in cDC2 phenotype to arrive at the claimed invention.
One of ordinary skill in the art would have been motivated to modify the teachings of Rosa to substitute the transcription factor PRDM1 for the transcription factor IRF8 since Zeng teaches that PRDM1 fates a dendritic cell towards a type 2 phenotype and IRF8 fates a dendritic cell towards a type 1 phenotype.
There would have been a reasonable expectation of success that the transcription factor PRDM1 could be substituted for the transcription factor IRF8 since Zeng teaches that PRDM1 is involved in fating a dendritic cell towards a type 2 phenotype.
Thus the cited art provides the requisite teachings and motivations to make and use the invention as claimed.
Response to Arguments
Applicant’s Arguments
Applicants argue in amendment that none of the cited references-alone or in any combination-teaches, suggests, or provides a reasonable expectation of success for employing PU.1 + IRF4 together with exactly one of PRDM1/POU2F2/TGIF1/RBPJ to reprogram or induce a cell into cDC2 using transduction and DC-supportive culture.
Under KSR V. Teleflex, 550 U.S. 398, 418 (2007), a §103 rejection requires an articulated rationale with a "reasoned" explanation for combining or modifying references, supported by evidence rather than hindsight.
Here, the office action asserts that Zeng's observation that PRDM1 is upregulated in naturally developing cDC2 provides motivation to substitute PRDM1 into Rosa's forced-expression reprogramming system. But Zeng provides only physiological expression correlations, not any suggestion to modify Rosa's transcription factor (TF) cocktail, much less to rewire its triad. This is precisely the type of hindsight-driven reasoning forbidden by KSR.
Rosa concerns methods for reprogramming fibroblasts into cDC1 cells, which are distinct from the cDC2 cells produced by process of claim 37. As indicated in Rosa, cDC1 and cDC2 cells represent functionally distinct dendritic cell lineages (Rosa et al., p.1 of 15, Introduction "Whereas cDC1 cells in antigen cross-presentation cDC2 cells prime CD4⁻ T cells presentation "). This distinction is further illustrated in Figure 1 of the present application as filed, where common dendritic cell progenitors (CDPs) differentiate into distinct DC subsets, including cDC1 cells that specialize in antigen cross-presentation via MHC class I molecules and triggering CTL responses, and cDC2 cells that specialize in MHC class II presentation and direct CD4+ T-cell polarisation toward Th2, Th17 and regulatory T-cell responses (paragraphs [0008] and [0016] of the US application as filed).
Rosa does not disclose or suggest the claimed IRF4-anchored triads or cDC2 induction. Rosa establishes a cDC1-biased direct-reprogramming system using PU.1 + IRF8 + BATF3 ("PIB"), yielding induced dendritic cells that align transcriptionally and functionally with cDC1 (e.g., XCR1, TLR3; cross-presentation) rather than cDC2. Rosa's single-cell/RNA-seq data, phenotyping, and functional assays consistently map the induced cells to cDC1, not cDC2. Crucially, Rosa itself shows that IRF4 is dispensable in its reprogramming framework: removal of IRF4 "did not have an impact" on reporter activation, and adding IRF4 does not compensate for loss of PU.1 or improve MHC-II expression. Rosa identifies PU.1, IRF8, and BATF3-not IRF4- as the essential triad for its system; removing any one of these essential factors reduces activity, while IRF4 does not serve as the required component.
The office action relies on a "substitute PRDM1 for IRF8" rationale (Office Action, p. 8). However, the Federal Circuit has held that "simple substitution" applies only when the elements are predictable and interchangeable. In re Fout, 675 F.2d 297 (CCPA 1982). Further, when the art teaches non-interchangeability, substitution is improper. See In re Ratti, 270 F.2d 810 (CCPA 1959). Transcription factor triads are not modular; Rosa demonstrates that they operate as a cooperative, integrated network relying on ETS-IRF interactions and a BATF3-IRF8 autoregulatory loop. Rosa teaches that IRF8 can be recruited through interaction with ETS transcription factors such as PU.1, that AP-1 factors such as BATF3 interact with IRF4 and IRF8 at composite binding sites, and that BATF3 binds the IRF8 super enhancer to maintain IRF8 expression via an autoregulatory loop. Removing IRF8 would therefore disrupt not only its direct transcriptional activity but also its interactions with PU.1 and the BATF3-IRF8 feedback circuit. Rosa further shows that individual overexpression of PU.1, IRF8 or BATF3, or even certain two factor combinations, is insufficient, and that even the optimized PU.1/IRF8/BATF3 combination yields relatively low reprogramming efficiency. These data confirm that Rosa's system is finely balanced and does not suggest that transcription factors can simply be swapped in and out like interchangeable modules. In parallel, the present application shows that the claimed PU.1/IRF4/PRDM1 system behaves as a tightly integrated network: removal of any one of PU.1, IRF4 or PRDM1 diminishes Clec9a reporter activation and CD11b expression, while individual expression of each factor results in only low levels of tdT and CD11b (paragraph [0251] of the US application as filed), and co-expression of additional factors such as IRF2 with PU.1, IRF4 and PRDM1 abolishes reporter activation (paragraph [0254] of the US application as filed).
Accordingly, Rosa neither discloses nor motivates the PU.1 + IRF4-anchored triads now claimed and teaches away from elevating IRF4 into an essential role in TF-driven DC reprogramming. Substituting out both of Rosa's required cDC1 drivers (IRF8 and BATF3) and replacing them with IRF4 plus PRDM1/POU2F2/TGIF1/RBPJ is not a "simple substitution" of one known element for another with predictable results; it is a complete rewiring of a non-modular, cooperatively acting triad that Rosa describes as tightly integrated (e.g., ETS-IRF pairing; AP-1/IRF composite motifs; BATF3 engaging the IRF8 super-enhancer to maintain IRF8). Rosa's data show that even partial perturbations reduce activity, confirming the lack of interchangeability and the unpredictability of outcomes upon triad changes. The office action's proposed simple substitution is not one-it is a complete re-architecture of a tightly-balanced triad, taught by Rosa to be sensitive to small perturbations.
In short, Rosa is a cDC1-reprogramming reference that (i) does not disclose cDC2 induction, (ii) does not disclose the claimed triads, and (iii) discourages reliance on IRF4 as an essential component-the opposite of what is required by claim 37. Rosa also doesn't make any suggestion to remove both IRF8 and BATF3 and replace them with IRF4 + PRDM1.
Zeng addresses physiological RA-dependent programming of intestinal DCs-not TF-driven reprogramming and cannot supply the missing teachings. Zeng dissects retinoic acid (RA) signaling in physiologic intestinal DC development from hematopoietic precursors and in RA-supplemented Flt3L/GM-CSF cultures; it documents RA's impact on subset balance (cDC2 representation) and transcriptomes in vivo/in vitro. Zeng does not disclose forced TF-expression-based reprogramming of somatic cells and does not teach using PU.1 + IRF4 plus exactly one of PRDM1/POU2F2/TGIF1/RBPJ to induce cDC2. At most, Zeng reports expression associations (e.g., IRF4; RA-responsive genes) in endogenous development-not actionable "recipes" for reprogramming with defined TF cocktails. Thus, Zeng provides no practical motivation or reasonable expectation of success for transforming Rosa's essential cDC1 triad (PU.1/IRF8/BATF3) into the claimed IRF4-anchored triads and obtaining cDC2 fate by transduction and DC-supportive culture.
Even if one were to identify cDC2-associated transcription factors from Zeng's expression profiling data, which Applicant does not admit, one of ordinary skill in the art starting from Rosa would not have any teaching to implement that information in practice as Rosa's entire experimental framework is specifically designed and optimised for cDC1 reprogramming. Hence, merely the knowledge that certain transcription factors such as IRF4 and PRDM1 are expressed in cDC2 cells during natural development does not on its own provide teaching on how to employ these factors in the context of reprogramming cells, and particularly does not provide any teaching to enable one to induce a cell into a conventional dendritic cell type 2, which is the opposite goal and established outcome of Rosa.
If proposed modification would render the prior art invention being modified unsatisfactory for its intended purpose, then there is no suggestion or motivation to make the proposed modification. In re Gordon, 733 F.2d 900, 221 USPQ 1125 (Fed. Cir. 1984). Rosa's clear desire and outcome is to generate cDC1 cells and that is exactly what Rosa produces. Substituting the essential triad of Rosa with PRDM1 as asserted by the office action to generate cDC2 cells as taught by Zheng would entirely render Rosa unsatisfactory for its intended purpose of producing cDC1 cells. As such, as commanded by the Court in In re Gordon, there is no suggestion or motivation to make the proposed modification to Rosa.
Deneault is an HSC expansion screen; it does not teach DC-subset reprogramming or the claimed triads. Deneault discloses an HSC "gene-activity regulator" screen (e.g., lists including Sfpil/PU.1, among many others) and provides vector/sequence information. It does not teach combining PU.1 with IRF4 and a third factor from PRDM1/POU2F2/TGIF1/RBPJ, does not teach DC-subset induction by forced TF expression, and does not address cDC2 reprogramming. As such, Deneault cannot supply the missing combination or the motivation to arrive at Applicant's IRF4-anchored triads for cDC2 induction.
Chicz is a translational-profiling/peptide resource; it does not disclose TF-cocktail reprogramming or DC-subset induction. Chicz concerns identifying peptides and nucleic acids from MHC-presented antigens, peptide arrays, and diagnostic utilities. It does not disclose cellular reprogramming, TF cocktails, or the use of PU.1 + IRF4 + PRDM1/POU2F2/TGIF1/RBPJ to induce cDC2. It is technologically orthogonal and therefore cannot bridge the specific TF-triad and cDC2-fate gaps in the §103 combination.
Jain focuses on PRDM1 (Blimp-1) in Th17/T-cell biology-not TF-driven DC-subset reprogramming. Jain is directed to modulating PRDM1 in Th17/T-cell contexts (EAE models; IL-23 signaling; BLIMP-1 antagonists/agonists), proposing therapeutic uses and screens. It does not disclose reprogramming non-DC cells into DC subsets by TF triads and does not suggest pairing PRDM1 with PU.1 + IRF4 for cDC2 induction. Therefore, Jain cannot supply the missing triad architecture or a reasoned expectation of success in the reprogramming context claimed.
The "simple substitution / predictable results" rationale is inapplicable to non-modular TF-triad reprogramming networks. (Office Action, p. 8.) The office action's assertion that the PU.1/IRF4/PRDM1 combination would be a simple substitution (e.g., "replace IRF8 with PRDM1") is inconsistent with the science and with Rosa's own findings. To arrive at the claimed PU.1/IRF4/PRDM1 combination from Rosa, the skilled person would need to remove IRF8, which Rosa teaches is essential, remove BATF3, which Rosa also teaches is essential, add IRF4 (despite Rosa's negative data), and introduce PRDM1, which is not mentioned in Rosa. This entails changing all three members of Rosa's essential three factor system. Such a reconstruction cannot reasonably be regarded as substituting a single known element for another with predictable consequences, particularly in a context as complex as transcription factor mediated lineage reprogramming. Given the teaching of the cited references in combinatoin, one of ordinary skill in the art would not have had a reasonable expectation that removing both IRF8 and BATF3, adding IRF4 (which Rosa deems non-essential), and introducing PRDM1/POU2F2/TGIF1/RBPJ would predictably produce cDC2 reprogramming.
The office action cites Deneault, Chicz, and Jain as "evidence" that TF sequences were known (Office Action, p.6-7). However, known sequences alone cannot supply missing motivation. In re Fine, 837 F.2d 1071, 1074 (Fed. Cir. 1988). They provide no teaching or motivation.
In contrast to the teaching of the cited references, the present specification provides detailed experimental evidence that PU.1, IRF4 and PRDM1 together induce Clec9a reporter activation and CD11b expression (paragraphs [0249]-[0251] of the US application as filed), confer MHC-II and CD45 expression and an antigen-presenting phenotype (paragraph [0253] of the US application as filed), drive TNF-a secretion and CD4+ T-cell proliferation (paragraphs [0257] and [0258] of the US application as filed) and resemble a pro-inflammatory cDC2B subset (paragraph [0259] of the US application as filed). These specific and advantageous technical effects are neither taught nor suggested by Rosa, Zeng or Deneault, Chicz and Jain alone or in combination.
Examiner’s Response
While Applicants arguments have been fully considered they are not found persuasive. The claimed method only requires two active steps and specifically regarding the transduction step has been amended to requires exactly three transcription factors, two of which are PU.1 and IRF4. Rosa uses PU.1 IRF4 and IRF8 and Applicant’s argue that removing IRF8 and replacing with PRDM1 would not be compatible with the teachings and results of Rosa and would not be a mere substitution. This argument is not found persuasive since the claimed invention is drawn to obtaining type 2 conventional dendritic cells and Zeng teaches clearly that IRF8 fates a dendritic cell towards type 1 and Blimp-1 (aka PRDM1) fates a cell towards type 2. At a minimum the ordinary artisan would find it obvious to try to substitute PRDM1 for IRF8 given the teachings of Zeng and if the goal is to fate cells towards a type 2 phenotype.
Applicant’s make the argument that transcription factors are not modular when functioning as a triad and Rosa teaches that their three transcription factors operate as a cooperative (via IRF8 functioning as a super enhancer) and thus simple substation of a single transcription factor such as PRDM1 for IRF8 is not obvious or predictable in view of Rosa’s teachings. Regarding the autoregulatory loop that Rosa discussed and Applicant argues, Rosa teaches:
“In this context, it was recently shown that BATF3 binds to the Irf8 super-enhancer
region, establishing an autoregulatory loop to maintain IRF8 levels after commitment to
the cDC1 lineage (9). However, because PU.1 and IRF8 overexpression is not sufficient to induce reprogramming, our results suggest that BATF3 may play additional roles during cDC1 specification”
In this regard, it should be emphasized that there is only a finite number of substitutions between the claimed combination of factors in claim 37 and the combination of factors in taught int the prior art of record. Rosa teaches that IRF8 is associated with maintaining a cDC1 phenotype and Zeng teaches that one specific factor, PRDM1, can specify a switch from a cDC1 to the claimed cDC2 phenotype. Thus it would be obvious to try the substitution of PRDM1 for IRF8 given the role of PRDM1 in directing a cell towards a type 2 phenotype as claimed.
Thus for the reasons above and of record the rejection is maintained.
Claim(s) 40 and 41 remain rejected under 35 U.S.C. 103 as being unpatentable over Rosa et al. (December 2018, Science Immunology, Vol. 3, pgs. 1-15, cited on IDS 8/24/2022) in view of Zeng et al. (2015, Mucosal Immunology, Vol. 9(1), pgs. 183-193, cited on IDS 8/24/2022) and evidenced by Deneault et al. (US 20090215875 A1), Chicz et al. (WO 2002/078524 A1) and Jain et al. (WO2013/070563 A1) as applied to claims 37-39 above, and further in view of Hayashi et al. (2000, Vaccine, Vol. 18, pgs. 3097-3105) for reasons of record in the Non-Final Office Action mailed on 12/1/2025 (and repeated below as amended).
Rosa and Zeng are relied upon above in teaching a method for reprogramming cells into cDC2 cells.
While Rosa teaches culturing their cells with exogenous IL-4 during reprogramming (pg. 12 col. 1 parag. 1), Rosa does not teach additionally transducing cells with at least one vector comprising a nucleic acid encoding an immunostimulatory cytokine, however this would be obvious in view of the teachings of Hayashi et al below.
Claim Definition: the specification teaches that immunostimulatory cytokines encompass IL-4 (parag. 194).
Regarding claims 40 and 41, Hayashi et al. teach transducing dendritic cells with a vector encoding IL-4 (see Abstract).
Specifically, Hayashi teaches:
“We reasoned that DC would serve as an ideal vector to deliver not only the antigen itself, but also a selected cytokine to the environment where the priming of naive T cells takes place. This concept has been tested recently by other investigators who introduced IL-12 or interferon-g (IFNγ) gene into short-term DC cultures by using viral vectors, as an attempt to improve the efficacy of DC-based vaccines to induce Th1-mediated immune responses [20-23]. No information, however, has been available with respect to the extent to which one can shift the immune responses toward Th2 by introducing the IL-4 gene to DC. In the present study, we introduced plasmid DNA encoding IL-4 into a long-term DC line to determine whether transient expression of IL-4 by relatively small numbers of DC would be sufficient to modify the immunological outcome of DC-based vaccines.” (pg. 3097 col. 2 parag. 2 bridge pg. 3098 col. 1 parag. 1).
Thus, at the time of filing the ordinary artisan would have found it prima facie obvious to combine the teachings of Rosa and Zeng regarding a method for reprogramming cells into cDC2 cells with the teachings of Hayashi regarding IL-4 stimulating dendritic cells to arrive at the claimed invention.
One of ordinary skill in the art would have been motivated to combine the teachings of Rosa/Zeng with the teachings of Hayashi teachings of Hayashi since Rosa teaches using exogenous IL-4 during their reprogramming method and Hayashi teaching that transducing dendritic cells with a plasmid vector encoding IL-4 allows dendritic cells to activate towards a Th2 subset
There would have been a reasonable expectation of success that the plasmid vector encoding IL-4 of Hayashi could transduce the cell of Rosa since Hayashi successfully transduces dendritic cells with a plasmid vector.
Thus the cited art provides the requisite teachings and motivations to make and use the invention as claimed.
Response to Arguments
Applicant’s Arguments
Applicants argue in amendment that the combination of Rosa, Zeng, Deneault, Chicz, Jain, and Hayashi fails to teach or suggest: (i) the specific three-TF reprogramming triads required by claim 37; (ii) the cDC2 lineage induction required by claim 37; and (iii) the additional cytokine-vector transduction requirements of claims 40-41. Because claim 37 is allowable for the reasons already set forth above and incorporated herein by reference, the dependent claims necessarily remain non-obvious. Moreover, the additional reliance on Hayashi does not cure the deficiencies in the primary combination.
Hayashi does not teach or suggest the claimed use of cytokine-encoding vectors in the
Context of TF-Driven cDC2 Reprogramming. The office action relies on Hayashi only for the
proposition that dendritic cells can be treated with cytokine-encoding vectors-specifically
IL-4-transduced DCs that modulate immunophenotype and cytokine responses. However,
Hayashi: (i) relates to modulating existing dendritic cells by transient IL-4 expression, not
reprogramming non-DC cells into a DC lineage; (ii) does not teach the use of PU.1/IRF4-anchored triads or anything analogous to the three-TF combinations required by claim 37; (iii) does not disclose combining cytokine-vector transduction with transcription-factor-mediated lineage conversion; and (iv) does not suggest using cytokine vectors in parallel with a TF-driven
cDC2-induction protocol. Instead, Hayashi examines how IL-4 secretion from IL-4-transduced
dendritic cells shifts the immune response (e.g., IgE levels, Th1/Th2 balance). This type of
immune-biasing experiment cannot supply the missing teachings required to make Applicant's
claims obvious. Therefore, Hayashi adds nothing that could supply the missing motivation or
expectation of success required to modify the already-deficient Rosa/Zeng/Deneault/Chicz/lain
combination.
Thus, even if one were to accept contrary to fact that the core reprogramming step of claim 37 were taught or suggested by Rosa/Zeng (it is not), Hayashi does not provide any motivation to apply cytokine-vector transduction to the specific reprogrammed cDC2 cells produced by the claimed triads, nor does it provide a reasonable expectation of success in doing so. Applicant respectfully requests withdrawal of the §103 rejection of claims 40 and 41.
Examiner’s Response
While Applicants arguments have been fully considered they are not found persuasive. Claims 40 and 41 do not require that the transduced IL-4 is required for reprogramming, only that that a nucleic acid encoding IL-4 is transduced along with the transcription factors in in claim 37. In this regard the teachings of Hayashi motivate the ordinary artisan to modify the teachings of Rosa and Zeng to include the further transduction of a nucleic acid encoding IL-4.
Thus for the reasons above and of record the rejection is maintained.
Conclusion
No claims are allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DAVID A MONTANARI whose telephone number is (571)272-3108. The examiner can normally be reached M-Tr 8-6.
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DAVID A. MONTANARI
Examiner
Art Unit 1632
/ANOOP K SINGH/Primary Examiner, Art Unit 1632
Prosecution Insights